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Aging is an important risk factor for the development of cardiovascular diseases, which can be accelerated by atherosclerosis, diabetes, hypercholesterolemia, or obesity. Vascular aging is mainly characterized by endothelial dysfunction, an alteration of endothelium-dependent signaling processes, and vascular remodeling. The underlying mechanisms include increased production of reactive oxygen species (ROS), inactivation of nitric oxide (·NO), and subsequent formation of reactive nitrogen and oxygen species (RNOS). Elevated RNOS may exhibit new messenger functions by posttranslational oxidative modification of intracellular regulatory proteins or lead to irreversible alterations of biological macromolecules. Various cellular sources may contribute to radical formation and are discussed in the context of the free radical hypothesis of aging. Clinically, endothelial dysfunction can be assessed by plethysmography, which may serve as an independent predictor for the risk of cardiovascular events. Current concepts in vascular aging, consequences for the development of cardiovascular events, and the particular role mitochondria may play in the development of RNOS-induced pathologic processes are discussed. [ABSTRACT FROM AUTHOR]